GLYCINE INCREASES ARTERIAL-PRESSURE AND AUGMENTS NMDA-INDUCED PRESSOR-RESPONSES IN THE DORSOMEDIAL AND VENTROLATERAL MEDULLA OF CATS

The present study is designed to determine and characterize two neurob iological events. Firstly, we investigated whether increases of system ic arterial pressure (SAP) and sympathetic vertebral nerve activity (V NA) produced by microinjection of glycine (Gly) in the dorsomedial (DM ) or rostral ventrolateral medulla (RVLM) are mediated by presser neur ons in DM or RVLM. Secondly, we assessed whether simultaneous microinj ections of Gly and N-methyl-D-aspartate (NMDA) in DM or RVLM potentiat e the NMDA-pressor effects. Changes in SAP and VNA were recorded in 33 cats under alpha-chloralose and urethane anesthesia. Microinjection o f sodium glutamate (Glu, 0.25 M, 30 nl) or Gly (1.0 M, 30 nl) into the DM or RVLM increased SAP and VNA in similar magnitude. Latencies of c hanges in SAP and VNA induced by Gly, however, were longer (3 s) than those induced by Glu. Prior microinjection of the following antagonist s blocked the Gly-induced presser responses: 2-amino-5-phosphonopentan oate (AP-5, 25 mM, 30 nl), a specific NMDA receptor antagonist; or glu tamate diethyl ester (GDEE, 0.5 M, 30 nl), a quisqualate receptor anta gonist; or kynurenic acid (KYN, 10 mM, 30 nl), a broad spectrum compet itive Glu antagonist. Prior treatment with strychnine (3 mM, 30 nl), a specific Gly antagonist, also blocked the Gly-induced presser respons es. Since Gly is believed to be an inhibitory neurotransmitter, these data suggest that Gly may produce presser actions via an inhibition on specific inhibitory neurons synapsing with the presser neurons. NMDA (0.1 M, 30 nl) and Gly (1.0 M, 30 nl) microinjected simultaneously in DM or RVLM produced a greater presser action than NMDA alone. This pot entiation was blocked by KYN, another known antagonist for such potent iation, but was only partially blocked by strychnine. (C) 1997 Elsevie r Science B.V.